Peripheral nerve injury is a common clinical disease. Effective post-injury nerve repair remains a challenge in neurosurgery, and clinical outcomes are often unsatisfactory, resulting in social and economic burden. Particularly, the repair of long-distance nerve defects remains a challenge. The existing nerve transplantation strategies show limitations, including donor site morbidity and immune rejection issues. The multiple studies have revealed the potential of tissue engineering strategies based on biomaterials in the repair of peripheral nerve injuries. We review the events of regeneration after peripheral nerve injury, evaluates the efficacy of existing nerve grafting strategies, and delves into the progress in the construction and application strategies of different nerve guidance conduits. A spotlight is cast on the materials, technologies, seed cells, and microenvironment within these conduits to facilitate optimal nerve regeneration. Further discussion was conducted on the approve of nerve guidance conduits and potential future research directions. This study anticipates and proposes potential avenues for future research, aiming to refine existing strategies and uncover innovative approaches in biomaterial-based nerve repair. This study endeavors to synthesize the collective insights from the fields of neuroscience, materials science, and regenerative medicine, offering a multifaceted perspective on the role of biomaterials in advancing the frontiers of peripheral nerve injury treatment.

Congenital myopathies (CMs) are a kind of non-progressive or slow-progressive muscle diseases caused by genetic mutations, which are currently defined and categorized mainly according to their clinicopathological features. CMs exhibit pleiotropy and genetic heterogeneity. Currently, supportive treatment and pharmacological remission are the mainstay of treatment, with no cure available. Some adeno-associated viruses show promising prospects in the treatment of MTM1 and BIN1-associated myopathies; however, such gene-level therapeutic interventions target only specific mutation types and are not generalizable. Thus, it is particularly crucial to identify the specific causative genes. Here, we outline the pathogenic mechanisms based on the classification of causative genes: excitation-contraction coupling and triadic assembly (RYR1, MTM1, DNM2, BIN1), actin-myosin interaction and production of myofibril forces (NEB, ACTA1, TNNT1, TPM2, TPM3), as well as other biological processes. Furthermore, we provide a comprehensive overview of recent therapeutic advancements and potential treatment modalities of CMs. Despite ongoing research endeavors, targeted strategies and collaboration are imperative to address diagnostic uncertainties and explore potential treatments.

We have reported that the phosphatidylinositol-3 kinase (PI3K)/Akt/RhoA signaling pathway mediates Wnt5a-induced cell migration of osteosarcoma cells. However, the specific receptors responding to Wnt5a ligand remain poorly defined in osteosarcoma metastasis. Wound healing assays were used to measure the migration rate of osteosarcoma cells transfected with shRNA or siRNA specific against ROR2 or indicated constructs. We evaluated the RhoA activation in osteosarcoma MG-63 and U2OS cells with RhoA activation assay. A panel of inhibitors of PI3K and Akt treated osteosarcoma cells and blocked kinase activity. Western blotting assays were employed to measure the expression and activation of Akt. Clonogenic assays were used to measure the cell proliferation of ROR2-knockdown or ROR2-overexpressed osteosarcoma cells. Wnt5a-induced osteosarcoma cell migration was largely abolished by shRNA or siRNA specific against ROR2. Overexpression of RhoA-CA (GFP-RhoA-V14) was able to rescue the Wnt5a-induced cell migration blocked by ROR2 knockdown. The Wnt5a-induced activation of RhoA was mostly blocked by ROR2 knockdown, and elevated by ROR2 overexpression, respectively. Furthermore, we found that Wnt5a-induced cell migration was significantly retarded by RhoA-siRNA transfection or pretreatment of HS-173 (PI3Kα inhibitor), MK-2206 (Akt inhibitor), A-674563 (Akt1 inhibitor), or CCT128930 (Akt2 inhibitor). The activation of Akt was upregulated or downregulated by transfected with ROR2-Flag or ROR2-siRNA, respectively. Lastly, Wnt5a/ROR2 signaling does not alter the cell proliferation of MG-63 osteosarcoma cells. Taken together, we demonstrate that ROR2 receptor responding to Wnt5a ligand activates PI3K/Akt/RhoA signaling and promotes the migration of osteosarcoma cells.

Background Muscle atrophy is a condition characterized by a decrease in muscle mass, and it is more common in women compared to men. Currently, there is limited research on the relationship between parity (number of pregnancies) and muscle atrophy. This study aims to investigate the association between parity and muscle loss in a population of Americans. Materials and Methods We collected clinical data from 3,530 participants in the National Health and Nutrition Examination Survey (NHANES) conducted between 2011 and 2018. Dose-response analyses using restricted quadratic spline models were employed to assess the association between parity and muscle atrophy in the study sample. Propensity Score Matching (PSM) was used to balance confounding variables between the muscle atrophy group and the non-muscle atrophy group. Results Among the 3,530 participants, 330 (9.3%) were diagnosed with muscle atrophy. Our study revealed that factors such as older age, Mexican American, low education level, marital status, poverty, physical inactivity, and higher parity were associated with muscle loss. The dose-response analyses using restricted quadratic spline models showed a positive correlation between parity and muscle atrophy in all patients, with an increased risk of muscle atrophy with higher parity. Additionally, the Propensity Score Matching analysis still demonstrated a positive association between parity and muscle atrophy after adjusting for other confounding variables. Conclusion Our study suggests that higher parity is associated with an increased risk of muscle atrophy in postmenopausal American women. Regular exercise may be effective in reducing the risk of muscle atrophy.